EFFECTS OF VITAMIN E ON MYOCARDIAL ISCHEMIC REPERFUSION INJURY IN DIABETIC RATS
- VernacularTitle:维生素E对糖尿病大鼠心肌缺血再灌注损伤的影响
- Author:
Junhai JIA
;
Suxian CHEN
;
Jianhua ZHAI
;
Fangfang HE
;
Yongchang CHEN
- Publication Type:Journal Article
- Keywords:
myocardial ischemic reperfusion;
diabetes;
intercellular adhesion molecule-1;
free radicals
- From:
Acta Nutrimenta Sinica
1956;0(02):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of vitamin E(VE) on the changes of the intercellular adhesion molecule-1(ICAM-1)and free radicals in ischemic-reperfused myocardium(MIR) of diabetic rats Method The diabetic rat model was established by i.p.streptozotocin injection.Four weeks later,MIR models were established,and 30 rats were divided into three groups with each group 10 rats(sham group,MIR group and VE group).The ICAM-1 protein expressions were evaluated by immunocytochemistry.The contents of malonialdehyde(MDA) in serum and myocardial tissues were detected.The activities of superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px) in serum and myocardial tissues were measured.The activities of Na+,K+-ATPase,Mg++-ATPase,Ca++-ATPase in myocardial mitochondria were measured.Results Compared with sham group,the activities of Na+,K+-ATPase,Mg++-ATPase,Ca++-ATPase in myocardial mitochondria were decreased,the contents of MDA in serum and myocardium increased,the levels of SOD and GSH-Px in serum and myocardium decreased,and the levels of ICAM-1 in myocardium increased significantly in MIR group.Compared with MIR group,the activities of Na+,K+-ATPase,Mg++-ATPase in myocardial mitochondria were increased,the levels of MDA in serum andmyocardium decreased the activities of SOD and GSH-Px in serum and myocardium increased,and the levels of ICAM-1 in myocardium decreased significantly in VE group.Conclusion VE could relieve myocardial ischemic reperfusion injury and the damage of lipid peroxidation and free radical induced by MIR in diabetic rats,and this effect was mediated by reduction of the expression of ICAM-1 protein.
